Fig. 6

Mitochondrial response to acute neuroinflammation. The model of the mitochondrial response to an acute neuroinflammatory environment proposed shows that the mitochondria respond at the tissue level by increasing their respiratory capacity and ATP production, whereas at the axonal level mitochondria respond by increasing their size and cristae complexity, although their transport is disrupted. Mitochondrial paralysis occurs early, before axonal damage is irreversible. Therefore, disruption of axonal mitochondrial transport (mainly retrograde) is a critical mechanism underlying mitochondrial dysfunction during neuroinflammation. Our results, and previous studies in this model [20], suggest that preserving axonal mitochondrial transport could represent a neuroprotective therapy for acute CNS inflammation